PECAM-1 (CD31) EXPRESSION IN THE CENTRAL-NERVOUS-SYSTEM AND ITS ROLE IN EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN THE RAT

The role of T cell activation associated adhesion molecules on lymphoc yte traffic and the initiation of inflammation has received considerab le attention. This study, using a new monoclonal antibody (mAb) TLD-3A 12, describes the distribution of PECAM-1 (CD31), an Ig supergene fami ly adhesion molecule thought to be important in leukocyte transmigrati on during inflammation, in rat lymphoid organs and spinal cord, PECAM expression within the CNS is confined to endothelial cells of the bloo d brain barrier (BBB), Induction of inflammation within the CNS using the adoptive transfer of myelin reactive CD4(+) T cells results in the de novo expression of immune adhesion and accessory molecules in the spinal cord, while the level of PECAM appeared only mildly increased. The distribution of PECAM on CNS endothelial cells became more diffuse during EAE induction, possibly the result of endothelial cell activat ion, In vitro studies demonstrate a partial inhibition of antigen-spec ific CD4(+) T cell proliferation following anti-PECAM mAb treatment, T reatment of Lewis rats with TLD-3A12 antibody prior to T cell injectio n and throughout EAE induction does not result in a delay in the onset of clinical signs or weight loss, nor does it decrease the incidence and severity of disease, These data suggest that the expression of PEC AM by CNS endothelial cells is not a requirement for the initiation of inflammation and clinical signs of EAE following the adoptive transfe r of encephalitogenic lymphocytes, Thus, cells requiring PECAM-1 to mi grate and perform their pathogenic functions are not critical to the d evelopment of rat EAE. (C) 1996 Wiley-Liss, Inc.